The Nuts and Bolts of Wound Care A Standardized Approach to Wound Evaluations
WINDY COLE, DPM ADJUNCT PROFESSOR AND DIRECTOR OF WOUND RESEARCH KENT STATE UNIVERSITY COLLEGE OF PODIATRIC MEDICINE The Problem
Aging population has lead to more patients with diabetes, obesity, vascular disease and chronic wounds
Wound care is a complex subspecialty that must take into account the multifactorial causes of chronic non-healing wounds
In order to ensure the best patient outcomes there are a multitude of patient parameters that must be evaluated
Today we will discuss an evidence-based approach to evaluating lower extremity ulcers The Problem
Medical advances in the 21st century have increased life expectancy
Patients are taking more medications than ever before
As a consequence of increased patient complexity we are now faced with the problem of difficult-to-heal wounds
*Nussbaum et al reports that 14% of Medicare beneficiaries have had at least 1 wound
Nussbaum SR et al An economic evaluation of the impact, cost, and Medicare policy implication of chronic nonhealing wounds. Value Health. 2018;21(1):27-32 The Problem
There is a need for education and training regarding proper wound care for all clinicians and medical personnel
Establish guidelines for evaluation, diagnosis, and appropriate wound care treatment plans
Ultimate goal is to provide safe, effective, efficient care in the office setting
Key is a holistic approach based on diagnosis, wound assessment, wound bed prep, treatment and follow up. Complete Medical History
Critical Items: Wound location Duration Trauma? Previous wound care, if any History of infection, antibiotics Hospitalization for wound/cellulitis Systemic risk factors; DM, PVD, PAD Pain Risk factors for venous or arterial disease; pain, selling, fatigue, clotting disorders Complete Medical History
Contributing factors to difficulty in healing wounds: Obesity Diabetes Infections Vascular disease Neuropathy Inflammatory/autoimmune states Malnutrition Nicotine use Renal dysfunction Edema Radiation
Medications
Medications affecting wound healing: Immunosuppressants Steroids Nonsteroidal anti-inflammatory agents Hydroxyurea-antimetabolite used to treat cancer Coumarins-blood thinners Methotrexate-immunosuppressive
Other Disease States
Other less common disease states can interfere with wound healing: Sickle cell disease Inflammatory bowel disease Rheumatoid arthritis Leukemia Thrombocytosis Cancer
Wound Examination
Wound Measurements Should be obtained at every visit Pre and Post debridement **Measure length, width and depth of wound in centimeters Wound Examination
Documenting wound appearance: Color and character of wound tissue Peri-wound tissue quality Nonviable tissue-necrotic, eschar, slough Dry or moist Moist necrotic tissue can harbor bacteria Granulation tissue, beefy red Rich in collagen and budding blood vessel Hypergranulation tissue May be a sign of neoplasm Epithelialization New skin growth Final stage of wound healing
Wound Examination
Wound exudate Amount Color Odor
Wound Examination Wound Etiology
Diagnosing wound etiology early and accurately is essential
Most common types of chronic wounds: Postoperative Traumatic Pressure Diabetic foot ulcers Venous leg ulcers Arterial ulcers Atypical wounds
Wound Etiology
Diabetic Foot Ulcers (DFUs) Commonly found on weight-bearing surfaces of the feet Result from increase plantar pressure May be covered or surrounded by callus Wound Etiology
Wagner Ulcer Classification Wound Etiology
Venous Leg Ulcers (VLUs) Typically found in the gaiter region of the leg Area extending from the ankle to below the knee Can be painful Usually edema present Heavy exudate Fibrotic wound base Wound Etiology
Arterial Ulcers Dry wound base Necrotic tissue Tight, shiny skin Scant or absent hair growth Very painful Cool-cold skin temp Wound Etiology
Pressure Ulcers Definition: localized damage to the skin and soft tissue over a boney prominence Staged according to depth and amount of tissue involved Stage 1: intact skin with nonblanchable redness Stage 2: partial thickness skin loss of epidermis Stage 3: full thickness skin loss with visible sub Q or fat Stage 4: full thickness skin loss with exposed bone, tendon or muscle Unstageable: covered with slough or eschar Not possible to determine deep tissue involvement Wound Etiology
Atypical Wounds: Crucial to determine etiology of wound that does not fit the major types and is non-healing Many disease processes can cause wounds Neoplasms Connective tissue disease Graft vs host Calciphylaxis Pyoderma gangrenosum
BIOPSY!! Inflow and Outflow
Arterial flow All patients with lower extremity wounds should be screened for arterial disease Ankle-brachial Index (ABI) Ankle (DP or PT) systolic pressure
Brachial artery systolic pressure
Inflow and Outflow
Venous leg ulcers (VLUS) represent the largest proportion of lower extremity ulcers VLUs effect 1% of the population Risk factors: DVTs Edema Varicose veins Venous stasis dermatitis
Infection
Most chronic wounds are colonized with bacteria Does the wound have clinic signs of true infection? Indication of invasive infection includes: Periwound induration Cellulitis extending >2cm beyond wound margins Increased local warmth Pain to palpation Fevers, chills, nausea Wound odor Increased drainage Friable or necrotic tissue Color changes to wound tissue Infection
Erythema: cellulitis or dependent rubor?
Infectious Disease Society Diabetic Foot Infection Classifications Infection
Infected wounds should be reassessed in 48-72 hours Most common cause of a previously improving wound to worsen is change in bacterial load Wound cultures Debridement
Goal of wound care is to create an environment favorable to wound healing Removal of necrotic or non-viable is essential Chronic wounds are stuck in a cycle of inflammation; regular debridement can transform wounds from chronic to active Traditional methods of debridement:
Surgical – scalpel, curette, etc., performed in the OR or clinic Autolytic – covers a wound with an occlusive dressing, intrinsic enzymes digest fibrosis, infection risk Enzymatic – collagenase, slow to act Maggot – green blow fly larvae, discriminate for necrosis and fibrosis Hydrosurgical – high pressure water, indiscriminate, bleeding risk Ultrasonic-Uses low-frequency ultrasound energy to remove unwanted, necrotic tissue
Neuropathy
*Diabetes is the most common cause of peripheral neuropathy Assessing foot sensation with a mono-filament Offloading
Relief of pressure from the wound is an important issue that needs addressed
Plantar foot ulcers result from abnormal foot pressures and repetitive stress
Pressure relieving footwear, removable cast walker, or total contact cast to off-load plantar foot pressure should be employed
• Removable cast walkers advantages: • allow access to wounds for bandage changes • can remove to sleep and shower.
• Potential downfall: • lack of forced compliance otherwise seen with TCCs
• Although studies show similar plantar pressure reduction for both, faster healing rates occur with TCCs Key Practice Pearls
The total contact cast (TCC) is the ideal method of off-loading for most patients
TCC use is supported by the highest level of evidence
Pressure and strain reduction are imperative in healing plantar foot ulcers
TCC is the gold standard for off-loading plantar foot ulcers
Total Contact Cast Pros Cons
Lack of product Ability to off load availability effectively Cost May also help to Training required reduce edema Lack of access to Insure appropriate wound patient compliance Contraindicated in infected wounds and severe PAD Indications: Contra-indications:
Wound must be non- Acute infection infected Severe ischemia Adequate blood supply to heal (ABI ≥ 0.7) Wagner grade 3 and 4
Wounds that do not probe Non-compliance with to tendon, capsule, or visits bone, or with abscesses Allergy to casting material
How TCCs Work
Off-loading Consensus Article
Total Contact Casting (TCC) is the preferred method for offloading diabetic plantar foot ulcers
TCC has most consistently demonstrated the best healing outcomes and is a cost-effective treatment
The likelihood of ulcer healing is increased with offloading adherence
Advanced therapeutics are unlikely to succeed in improving wound healing outcomes unless effective offloading is obtained
Compression
Compression is key to treating most lower leg ulcers
40% of women an 17% of men are reported to have venous insufficiency
Compression should reduce edema at the maximum level the patient can tolerate
Venous Insufficiency
Improper functioning of the valves in the veins of the legs cause insufficient amounts of blood to be pumped back to the heart.
It is neither uncommon or benign
Major cause of skin disorders, edema and lower extremity ulcerations
Usually gets worse over time Venous Insufficiency Compression
*Graduated compression therapy can reduce vessel diameter and redirect blood centrally, reduce edema, and improve arterial circulation
*There is evidence that compression can decrease destructive proteases and inflammatory cytokines that contribute to ulceration Compression There are basically two different forms of compression therapy
―Non Elastic: these bandages only have an effect during movement, when contraction and relaxation of the muscles cause volume changes of the extremities. (Unna’s boot)
―Elastic: these bandages adjust to the volume changes of the extremity, and by their elastic tension exert continuous pressure on the surface of the skin. (MLCT) Partsch H, Menzinger G, Mostbeck A. Inelastic leg compression is more effective to reduce deep venous refluxes than elastic bandages. Dermatol Surg. 1999;25:695-700.
Elastic Material (long-stretch)
Multicomponent Multilayer: (short/long-stretch)
Non Elastic Material: (short-stretch)
Partsch H, Menzinger G, Mostbeck A. Inelastic leg compression is more effective to reduce deep venous refluxes than elastic bandages. Dermatol Surg. 1999;25:695-700.
Congestive Heart Failure
Patients with decompensated heart failure may receive compression therapy with caution because compression therapy redistributes blood towards the center of the body, thereby increasing the pre-load of the heart and possibly causing further overload and or even death.
Weingarten M. State-of-the-art treatment of chronic venous disease. Clin Infect Dis. 2001;32(6):949-954. Pascarella L, et al. Venous hypertension and the inflammatory cascade: major manifestations and trigger mechanisms. Angiology. 2005;56:S3-S10.
Compression
Any Questions?